Thromboxane Mediates the Increase in Alveolar Surfactant Pool Induced by Free Fatty Acid Infusion in the Rabbit

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Abstract
I.v. infusion of free fatty acid (FFA) produces pulmonary edema and an increase in the alveolar surfactant content of the rabbit. In order to identify a likely mediator of this lung response to FFA, we used inhibitors of cyclooxygenase (indomethacin, 15 mg/kg i.v., or meclofenamate, 5 mg/kg i.v.) and thromboxane synthetase inhibitors (imidazole, 50 mg/kg i.v. or dazoxiben, 2 mg/kg i.v.) which were administered before FFA, 20 mg/kg per min i.v., in 4 different experimental series (n = 54). Lung surfactant was measured in bronchial-alveolar lavage fluid by determining disaturated phosphatidylcholine (DSPC). Both kinds of inhibitors blocked the increase in FFA-induced DSPC. They increased the survival rate but they only slightly changed the post-FFA morphofunctional pulmonary alterations. Apparently, the increase in alveolar surfactant induced by FFA is likely mediated by thromboxane. This mediator would seem to play a minor role in the FFA-induced pulmonary edema observed.